I know what you’re thinking, a hypothermia blog in June? As peak trauma season approaches and winter can’t decide if it wants to go or stay, I think this is an excellent time to start refreshing our knowledge on trauma. I am a firm believer in learning from our past and using evidence-based practice to lead the future. With that, I want to understand why I am doing something.
The “golden hour” was coined by Dr. Adams Cowley who implemented one of the first clinical shock trauma centers at the University of Maryland. He defined this Golden Hour as the moment of injury to the time of definitive treatment. Because this hour was so important based on Dr. Cowley’s research, he coordinated with the Maryland State Police Aviation Department to transport the first severely injured civilian by helicopter in March of 1970. (4) I know, super exciting. Keep reading, I promise I’m almost done nerd-ing out on the history stuff.
The golden hour these days is not a specific time frame as currently, it has become a controversial topic related to the validity of the 60 minutes. However, looking beyond the 60 minutes we must identify lethal attributes during our assessments and move with urgency. When a person gets injured, they will have a multitude of factors that occur as a result of their injury. With a physical assault on our body’s homeostasis, we begin to develop irreversible damage to our body from coagulopathy, acidosis, and hypothermia. The Triad of Death.
Knowing the lethal Trauma Triad of Death is the root of the interventions that we utilize today. The triad consists of hypothermia, coagulopathy, and acidosis. While this triad of death is more like a vicious circle where one affects the other two and vice versa, each component of the Triad of Death is significant to the ultimate demise of our multi-system trauma patient. I think that each component deserves its own spotlight, but today we will be focusing on hypothermia. While Acidosis and coagulopathy are monsters in and of themselves, I interpret hypothermia as a big instigator. With decreasing core temperatures, comes increasing acidosis and coagulopathy issues. The coolest part, we as EMS and in-hospital providers are more than capable of identifying hypothermia, hypothermic conditions, and implementing time-critical interventions to stop and reverse hypothermia. That’s Baller -- Let’s try to organize this chaos!
Word of the day: Endotherms (don’t worry, I just learned this word too and I will probably forget it by the time I finish reading this blog). Endotherms have the ability to thermoregulate regardless of what kind of external environment they are in. Humans, other mammals, and birds are endotherms. To ensure proper bodily function (farts included), adequate volume and cardiac function must be present. Thermoregulation by definition is our body’s ability to maintain a tightly regulated body temperature independently, regardless of external factors. Normothermia range is 35.6-37.8C, with 37C being identified as the body’s most optimal internal temperature to function (4).
The hypothalamus in the brain is the center for thermoregulation. The hypothalamus is located, in an effort not to go too in-depth, is in your brain 🧠 🤯. The hypothalamus has many functions and thermoregulation is one of them. The hypothalamus controls thermoregulation by sensing the temperature of the blood as the blood passes by the hypothalamus, and also by signals sent from our nerves in our skin and sent up the spinal cord to the hypothalamus.
The Hypothalamus provides negative feedback. A decrease in the body’s temperature signals the hypothalamus to do its magic. Aerobic cellular respiration produces 36 ATP(energy). With that process, heat is also produced and then carried via the bloodstream to warm the body. When a decrease in temperature is detected, the hypothalamus signals an increase in heat production and transport of the heat by activating our sympathetic nervous system, increasing cardiac output, and activating muscles to shiver. The sympathetic nervous system (SNS) is activated with the goal to conserve heat and provide heat to our vital organs. The SNS does this with peripheral vasoconstriction and increasing cardiac output. With peripheral vasoconstriction, blood is pulled away from the skin and thus conserves heat by minimizing the heat lost through the skin. This also shunts blood to the core, providing heat to vital organs. Increasing cardiac output allows the blood to transport glucose, oxygen, and heat produced from the increased basal metabolic rate. Muscle stimulation produces piloerector muscles (goosebumps) and shivering to produce heat. This is a major source of heat production. One of the negative effects of shivering is the increased consumption of oxygen and glucose to produce these “shivers''.
Cellular Effects of Hypothermia
in Conjunction with Trauma
Fun Fact: patients with trauma and a documented core temperature of <90 F (32.2 C) have a mortality rate as high as 100% compared to those of non-trauma-related hypothermia (7). As just discussed, the hypothalamus does a great job at thermoregulating. However, when trauma is involved, there becomes an added obstacle of decreased blood volume that the body now has to work extra hard at to overcome
Decreasing blood loss contributes to the decrease in the amount of oxygen, glucose, and heat that is available to the body. The body has been stripped away of its prime heat source: BLOOD 🩸. Now the body is not only not capable of transporting the supplies needed for metabolism, but also not able to transport what little heat was produced with metabolism.
Traumatic head injuries not only affect our neurologic system but have the potential to affect how we respond to hypothermia. With an injury to our head, we are at risk of not being able to efficiently thermoregulate because remember that the hypothalamus is located in the brain. Brain bleeds can cause increased intracranial pressure which could put pressure on our hypothalamus, or more likely, impede blood flow to our hypothalamus causing a decrease in response.
Spinal injuries: The hypothalamus relies on afferent signals from the body to detect a decreasing temperature. It also relies on the ability to send out signals to the body to initiate responses to thermoregulation. With spinal injuries, we now have a roadblock at the level of injury impeding those signals to help regulate our body temperature.
Cardiac function is also affected by hypothermia. Initially, cardiac output increases in an attempt to help with thermoregulation. But as temperatures drop, bradycardia progresses due to the decreased spontaneous depolarization of pacemaker cells and lack of oxygen and glucose stores available. Osborn waves (AKA, J waves) are characteristically seen in hypothermia but are not specific to hypothermia. Osborn waves are noted at the J point and described as a positive deflection with a characteristic hump. Other ECG abnormalities that can be noted are bradyarrhythmia and prolonged QT intervals. Bradyarrhythmias, prolonged QT intervals, and early repolarization noted on ECGs are preceded by lethal arrhythmias such as ventricular tachycardia/fibrillation as hypothermia continues and worsens. It is thought that ECG changes are attributed to the increasing acidosis, delayed electrolyte fluctuation, and ischemia (6).
Hypothermia in Relation to Acidosis
As the body attempts to maintain normothermia, an initial increase in basal metabolic rate (BMR) causes an increase in the consumption of glucose. If not rapidly identified and treated, the body will exhaust all glucose stores in an attempt to thermoregulate. With hemorrhagic shock and poor oxygen perfusion to the tissues, the body will still attempt to create energy by converting to anaerobic metabolism, which we all know is a piss poor way to produce ATP (energy). Anaerobic metabolism produces the bi-product of lactic acid. As perfusion worsens and glucose is depleted, the accumulation of lactic acid contributes to the worsening metabolic acidosis (7).
Hypothermia in Relation to Coagulopathy
Coagulation, specifically complex enzymatic reactions of the clotting cascade, is dependent on normothermic conditions among other things. In a normothermic patient, coagulation occurs normally, and the ability to form clots to stop internal and external hemorrhage ensues. However, when the body begins to decrease in core body temperature, the effects of impaired clotting efficiency are noted. The body now struggles to stop the bleeding due to impaired platelet function, inhibition of clotting factors and inappropriately breaking down clots, which are hypothermic induced. Coagulopathy is reversible with patient rewarming. "HOLD. THE. PHONE!" Yes, you read that right. This is important for two reasons. One, we as first responders are capable of stopping and potentially improving coagulopathy issues. The second, when running coagulation studies, standard practice is to prewarm the blood sample to 37C prior to running the studies. What does that mean you ask? If warming the patient up reverses coagulopathy, warming blood samples up can also normalize lab samples and give false results.
Interventions to Mitigate Hypothermia
Here is where we shine folks: INTERVENTIONS. Or, the bread and butter of stopping and reversing hypothermia. When it comes to hypothermia and trauma, the number one intervention to mitigate the Triad of Death; STOP THE BLEED. Pack the wound, apply pressure, or place a tourniquet. Remember it’s the little things that matter. Our small but mighty interventions also include early temperature management -- don’t just wait for the back of the ambulance or for the Bair Hugger at the hospital. It’s ok to be a Rescue Randy on scene and pull out that foil blanket you carry around with you in your fanny pack… you know some of you are guilty (* COUGH... 💙 Taylor 💙 ...COUGH*). Remove the patient from a cold environment as soon as possible. Remove wet/bloody clothes, while doing your assessment, and replace them with warm blankets. Calling in a trauma alert to the receiving facility can allow the trauma team to ready their equipment including the Bair Hugger, rapid infusers (which include heating mechanisms), and time to crank the heat up in their trauma rooms.
For you advanced providers, when starting crystalloids or colloids, administer them warm. During RSI, remember that when giving sedatives and paralytics, we take away the patient’s ability to shiver, which is removing one of the biggest compensators for hypothermia. If you have the capability, continuous temperature monitoring either front-loaded or back-loaded (esophageal or rectal) will allow you to obtain an accurate continuous core temperature measurement. These all seem like small minor details but when added up they can make a huge impact on inpatient care.
We as providers have the ability to impact our patient's care. Hypothermia is just one of the contributors to the demise of our trauma patients. Just because we focused on hypothermia today, doesn’t mean that acidosis, coagulopathy (and hypocalcemia) are not important. You might be asking yourself why hypocalcemia was just referenced?.. Recently there has been data to support a 4th critical criterion that contributes to the multisystem trauma patient. This has been referred to as the Diamond of Death. FOAMfrat just had a great blog on hypocalcemia and trauma put out by Mike Brown. Go check it out, here is the LINK! By critically thinking about what is going on with our patients, and the why behind it, we can implement our interventions appropriately. We are not only able to improve our patient’s outcomes, but we are also able to decrease mortality, morbidity, and permanent disability. (Take that insurance company!)
Brittany Grandfield, A Handful of Letters, RN.